Singh A, Abraham Wickliffe C
Department of Psychology, Brain Health Research Centre, Brain Research New Zealand, University of Otago, Box 56, Dunedin, 9054, New Zealand.
Exp Brain Res. 2017 Jun;235(6):1645-1655. doi: 10.1007/s00221-017-4928-1. Epub 2017 Mar 15.
Activity-dependent synaptic plasticity phenomena such as long-term potentiation and long-term depression are candidate mechanisms for storing information in the brain. Regulation of synaptic plasticity is critical for healthy cognition and learning and this is provided in part by metaplasticity, which can act to maintain synaptic transmission within a dynamic range and potentially prevent excitotoxicity. Metaplasticity mechanisms also allow neurons to integrate plasticity-associated signals over time. Interestingly, astrocytes appear to be critical for certain forms of synaptic plasticity and metaplasticity mechanisms. Synaptic dysfunction is increasingly viewed as an early feature of AD that is correlated with the severity of cognitive decline, and the development of these pathologies is correlated with a rise in reactive astrocytes. This review focuses on the contributions of astrocytes to synaptic plasticity and metaplasticity in normal tissue, and addresses whether astroglial pathology may lead to aberrant engagement of these mechanisms in neurological diseases such as Alzheimer's disease.
诸如长时程增强和长时程抑制等活动依赖的突触可塑性现象是大脑中存储信息的候选机制。突触可塑性的调节对于健康的认知和学习至关重要，这部分是由元可塑性提供的，元可塑性可以在动态范围内维持突触传递，并可能预防兴奋性毒性。元可塑性机制还允许神经元随着时间整合与可塑性相关的信号。有趣的是，星形胶质细胞似乎对某些形式的突触可塑性和元可塑性机制至关重要。突触功能障碍越来越被视为阿尔茨海默病（AD）的早期特征，且与认知衰退的严重程度相关，而这些病理变化的发展与反应性星形胶质细胞的增加有关。本综述重点关注星形胶质细胞在正常组织中对突触可塑性和元可塑性的贡献，并探讨星形胶质细胞病变是否可能导致这些机制在诸如阿尔茨海默病等神经疾病中异常激活。
